Effects of maternal hyperoxygenation on atrioventricular velocity waveforms in healthy and growth-retarded fetuses.
In order to assess whether maternal hyperoxygenation induces modifications of Doppler-measured velocity waveforms across atrioventricular valves, 15 healthy and 15 growth-retarded fetuses were studied in basal conditions and during the maternal administration of 60% humidified oxygen. Recordings were performed at 5-min intervals before, during and after maternal oxygen administration. In basal conditions, growth-retarded fetuses exhibited significantly lower ratios between the velocities during early passive ventricular filling and active ventricular filling (E/A ratio) at the level of both mitral and tricuspid valves when compared to healthy fetuses. Furthermore in healthy fetuses the velocity time integral across the tricuspid valve always slightly exceeded that across the mitral valve, whilst growth-retarded fetuses showed an inversed ratio between these velocities. During oxygen administration no changes were found between the two groups of fetuses with regard to the E/A ratios. Similarly the velocity time integrals were unaffected by oxygen administration in the healthy fetuses. Besides growth-retarded fetuses exhibited significant temporary modifications during oxygen administration as expressed by an increase in the velocity time integral across the mitral valve associated with a decrease of that across the tricuspid. These changes result in an inversion of the ratio between transtricuspid and transmitral velocity time integrals reaching values similar to those of healthy fetuses. Short-term oxygen administration affects the intracardiac flow redistribution present in growth-retarded fetuses bringing it to a pattern similar to that of healthy fetuses whereas the E/A ratios were not affected by the treatment.
Rizzo
G
G
Department of Obstetrics and Gynecology, S. Cuore Catholic University, Rome, Italy.
Arduini
D
D
Romanini
C
C
Mancuso
S
S
D001775:Blood Circulation; D001783:Blood Flow Velocity / Q000187:drug effects; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005333:Fetus / Q000502:physiology*; D006325:Heart Atria; D006351:Heart Valves / Q000503:physiopathology; D006352:Heart Ventricles; D006801:Humans; D010100:Oxygen / Q000097:blood* / Q000494:pharmacology; D011247:Pregnancy; D012016:Reference Values; D014463:Ultrasonography
D010100:Oxygen